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Am J Physiol Gastrointest Liver Physiol 284: G385-G391, 2003. First published November 13, 2002; doi:10.1152/ajpgi.00049.2002
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Vol. 284, Issue 3, G385-G391, March 2003

Exposure to schistosome eggs protects mice from TNBS-induced colitis

David E. Elliott1, Jie Li1, Arthur Blum1, Ahmed Metwali1, Khurram Qadir1, Joseph F. Urban Jr.2, and Joel V. Weinstock1

1 Department of Internal Medicine, Division of Gastroenterology-Hepatology, University of Iowa College of Medicine, Iowa City, Iowa 52242; and the 2 Immunology Disease Resistance Laboratory, Animal and Natural Resources Institute, Agricultural Research Service, United States Department of Agriculture, Beltsville, MD 20705

Crohn's disease results from dysregulated T helper (Th)1-type mucosal inflammation. Crohn's disease is rare in tropical countries but prevalent in developed countries with temperate climates, in which its incidence rose after 1940. In contrast, exposure to helminthic parasites is common in tropical countries but is rare in developed countries. Helminthic parasites induce immunomodulatory T cell responses in the host. We hypothesize that immunomodulatory responses due to helminths may attenuate excessive Th1-type inflammation. To test that hypothesis, mice were exposed to eggs of the helminth Schistosoma mansoni and then challenged rectally with trinitrobenzesulfonic acid (TNBS) to induce colitis. Schistosome egg exposure attenuated TNBS colitis and protected mice from lethal inflammation. Schistosome egg exposure diminished IFN-gamma and enhanced IL-4 production from alpha CD3-stimulated spleen and mesenteric lymph node cells of TNBS-treated mice. Schistosome egg exposure decreased colonic IFN-gamma but increased IL-10 mRNA expression in TNBS-treated mice. Intact signal transducer and activator of transcription 6 was required for attenuation of colitis. Exposure to helminths can decrease murine colonic inflammation.

Schistosoma mansoni


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